Recent quotes:

Nearly two billion adults worldwide are overweight, more than 600 million of whom are obese. In addition to increasing risk of conditions such as diabetes and heart disease, obesity is also a known risk factor for cognitive disorders including Alzheimer's disease. The cellular mechanisms that contribute to cognitive decline in obesity, however, are not well understood.
Elise Cope and colleagues replicated previous research by demonstrating diet-induced obesity in mice impairs performance on cognitive tasks dependent on the hippocampus and results in loss of dendritic spines -- the neuronal protrusions that receive signals from other cells -- and activates microglia. Using genetic and pharmacological approaches to block microglial activity, the researchers established microglia are causally linked to obesity-induced dendritic spine loss and cognitive decline. The results suggest obesity may drive microglia into a synapse-eating frenzy that contributes to the cognitive deficits observed in this condition.

Insulin gives an extra boost to the immune system -- ScienceDaily

"We have identified one of metabolism's most popular hormones, specifically the insulin signaling pathway, as a novel 'co-stimulatory' driver of immune system function," says Dr. Dan Winer, who is also Assistant Professor, Department of Laboratory Medicine and Pathobiology at University of Toronto. "Our work characterizes the role of this signaling pathway in immune cells, mainly T cells, opening up avenues in the future to better regulate the immune system."

Can You Cure Lyme disease? The Controversy Around Diagnosis and Treatment

In my experience, 18 months of ozone therapy was the magic bullet against Lyme disease. Ozone inactivates bacteria, viruses, fungi, yeast and protozoa by breaking through the cell wall which weakens the cell, making way for your own immune cells to move in and do their thing. It also uses extra oxygen to activate the immune system.[8] You’ll need a functional medicine doctor to put you on a program.
If you’re frustrated by Lyme disease or any chronic illness, join the club. But, don’t stay for long. The best thing you can do is arm yourself with information and seek the guidance of medical professionals who are qualified and experienced in treating the tough stuff. It takes work, but you’ll come out on the other side stronger than ever.

The immune system and the pathogenesis of depression

There is bidirectional communication between the HPA axis and the immune system. Cytokines activate the HPA axis and thus lead to the release of cortisol, the stress hormone, which ordinarily suppresses the immune response. Cortisol also inhibits its own release and thus the body is able to maintain a stable immune response through a tightly regulated feedback inhibition system. This regulation mechanism seems to be dysfunctional in depressive disorders and is thought to occur because of cytokine mediated receptor resistance to cortisol, thus impairing feedback inhibition. This essentially means that cytokines make cortisol unable to act on the receptors that would inhibit its release. Long story short — the HPA axis is hyperactive because of cytokines, leading to a chronic stress response because cytokines impair the body’s ability to regulate it — thus leading to depressive symptoms.

Probiotic Shot May Alleviate Brain Stress | GEN

Studies have also shown that patients with anxiety- and trauma-related conditions have reduced numbers of regulatory T cells (Tregs, while research also suggests that trauma, illness, or surgery can sensitize certain regions of the brain to mount an inflammatory response to subsequent stressors, which can lead to mood disorders.
“There is a robust literature that shows if you induce an inflammatory immune response in people, they quickly show signs of depression and anxiety," says lead author Matthew Frank, Ph.D., a senior research associate in the department of psychology and neuroscience. "Just think about how you feel when you get the flu."

Beyond killing tuberculosis: How can we tolerate an infection without eliminating a pathogen? -- ScienceDaily

"In contrast to conventional thinking, we show that T cells are essential for regulating the body's toler-ance to Mtb infection," explains one of the study's first authors, Dr. Nargis Khan, who is currently a postdoctoral fellow in Dr. Divangahi's lab at the RI-MUHC.
Giving the widespread drug resistance to various Mtb strains the limited pipeline of effective antibiotics and the lack of an efficient vaccine, alternative approaches to treat TB are urgent. "If we could understand the mechanisms of 'natural immunity' that controls TB in 90-95 per cent of infected individuals," says Dr. Divangahi,"we will able to design a novel therapy or vaccine to substantially reduce the world wide burden of this ancient disease."

A gut bacterium's guide to building a microbiome: Unlike invading pathogens, which are attacked by the immune system, certain good bacteria in the gut invite an immune response in order to establish robust gut colonization -- ScienceDaily

The particular species is found abundantly in the large intestines of many mammals, including humans, and was previously shown by the Mazmanian lab to protect mice from certain inflammatory and neurological disorders such as inflammatory bowel disease and multiple sclerosis. Interestingly, though there are multiple strains of B. fragilis, healthy people form a long-term, monogamous relationship with only a single strain.
"Studies by other labs have shown that most people carry the same strain of B. fragilis throughout their lives," says Donaldson. "We wanted to understand at a molecular level how these bacteria are able to colonize the gut in a stable, long-term way."
First, the researchers aimed to examine B. fragilis's symbiotic relationship with the gut by physically looking at the locations where the bacteria reside. Using electron microscopy imaging on samples of mouse intestines, the team was able to see that B. fragilis clumps together in aggregates deep within the thick layer of mucus lining the gut, nestled close to the epithelial cells that line the surface of the intestine. Donaldson and his collaborators theorized that this spatial niche is necessary for a single species to settle in and establish a stable foothold.
The team next aimed to determine what mechanisms allow B. fragilis to colonize such a niche within the gut. They found that each B. fragilis bacterium is encased in a thick capsule made of carbohydrates. The capsule is typically associated with pathogens (bad bacteria) attempting to cloak themselves from recognition by and attack from the body's immune system. Mutant bacteria lacking this capsule cannot aggregate and do not inhabit the mucosal layer. Thus, the researchers theorized that capsular carbohydrates are necessary for B. fragilis strains to monopolize their niche in the gut.
Because bacterial capsules were known to be related to an immune response in pathogenic bacteria, Donaldson and Mazmanian hypothesized that there may also be an immune response to the B. fragilis capsule. Indeed, they found that antibodies, immune proteins that grab onto and mark specific bacteria or viruses for other immune cells to engulf and destroy, were binding to the B. fragilis capsule in the intestine. One particular kind of antibody, immunoglobulin A or IgA, is found throughout the gut -- in fact, it is the most abundantly produced type of antibody in humans -- but its specific functions have been enigmatic.

Drinking baking soda could be an inexpensive, safe way to combat autoimmune disease: A daily dose of baking soda may help reduce the destructive inflammation of autoimmune diseases like rheumatoid arthritis, scientists say. -- ScienceDaily

Drinking baking soda, the MCG scientists think, tells the spleen -- which is part of the immune system, acts like a big blood filter and is where some white blood cells, like macrophages, are stored -- to go easy on the immune response. "Certainly drinking bicarbonate affects the spleen and we think it's through the mesothelial cells," O'Connor says.
The conversation, which occurs with the help of the chemical messenger acetylcholine, appears to promote a landscape that shifts against inflammation, they report.

'Mono' virus linked to 7 serious diseases: Epstein-Barr virus may affect health in more ways than known -- ScienceDaily

The new paper shows that seven seemingly unrelated disease states actually share a common set of abnormal transcription factors, each affected by the EBNA2 protein from the Epstein-Barr virus. When these EBNA2-related clusters of transcription factors attach themselves to one portion of the genetic code, the risk of lupus appears to rise. When those same transcription factors land on another part of the code, the risk of multiple sclerosis appears to rise. And so on.
"Normally, we think of the transcription factors that regulate human gene expression as being human," Kottyan says. "But in this case, when this virus infects cells, the virus makes its own transcription factors, and those sit on the human genome at lupus risk variants (and at the variants for other diseases) and that's what we suspect is increasing risk for the disease."

“The lining of the brain, with help from the immune system, has a remarkable ability to put itself back together again after injury,” said Dorian McGavern, Ph.D., scientist at the NIH’s National Institute of Neurological Disorders and Stroke and the senior author of the study published in Nature Immunology. “As we learn more about all the cells involved in the repair process, we may be able to identify potential targets for therapy that lead to better outcomes for patients.”
The study came about from an observation on MRI scans of adult patients who experienced a concussion or mTBI. Around half of patients with mTBI show evidence of injury to blood vessels in the meninges, which appears on MRI scans as a vascular dye leaking out of the damaged vessels.
The meninges are a collection of membranes that line the central nervous system and help protect brain and spinal cord tissue from various forms of injury. Damage to the meninges can cause cell death in underlying brain tissue.

Treatable Immune System Disorder Could Be Mistaken For Schizophrenia or Bipolar Disorder - Neuroscience News

The study was inspired by the 2007 discovery of anti-NMDA receptor encephalitis, a disease that causes symptoms similar to schizophrenia or bipolar disorder but can be treated with existing immunotherapy medications.
“We suspect that a significant number of people believed to have schizophrenia or bipolar disorder actually have an immune system disorder that affects the brain’s receptors,” said Joseph Masdeu, M.D., Ph.D., the study’s principal investigator and a neurologist with the Houston Methodist Neurological Institute. “If true, those people have diseases that are completely reversible – they just need a proper diagnosis and treatment to help them return to normal lives.”

Researchers Find Missing Link Between the Brain and Immune System - Neuroscience News

Instead of asking, ‘How do we study the immune response of the brain?’ ‘Why do multiple sclerosis patients have the immune attacks?’ now we can approach this mechanistically. Because the brain is like every other tissue connected to the peripheral immune system through meningeal lymphatic vessels,” said Jonathan Kipnis, PhD, professor in the UVA Department of Neuroscience and director of UVA’s Center for Brain Immunology and Glia (BIG). “It changes entirely the way we perceive the neuro-immune interaction. We always perceived it before as something esoteric that can’t be studied. But now we can ask mechanistic questions.”

Why the 'Worst' Crypto Networks Will Be The Biggest - CoinDesk

These crypto networks will have a familiar failure pattern:
A well-meaning protocol designer comes in and looks at a complex reality.
They don't understand how it works because it's complex and messy.
Rather than trying to understand why it looks like a mess and whether that is serving some deeper purpose, they attribute it to the current design being "irrational, ugly and inelegant"
They come up with an idealized protocol design which makes sense on paper
After the initial marketing hype and buzz fades away, the protocols users and community don't like "living there" and slowly migrate away.

Why do healthy children die from the flu? Study offers new insights -- ScienceDaily

The study examined specific immune pathways known to be activated during flu infections in both humans and mice, which makes the findings relevant to children. Coates and colleagues focused on the initial immune response to the flu, using healthy adult and young mice who have not had previous exposures to the virus. They discovered that in the young, more immune cells called monocytes were recruited to the lungs, and that the gene expression profiles of these cells had more inflammatory features, causing greater inflammation and more severe lung injury.
"Our findings provide new targets for developing effective medicines to treat the flu in children," says Coates. "We can seek ways to prevent monocytes from coming to the lungs, or we can target monocyte behavior in the lungs to reduce dangerous inflammation."

"We were able to show that opioid agonists activate opioid receptors on immune cells, which triggered the release of endogenous painkillers (opioid peptides) and produced analgesia in a mouse model of neuropathic pain," explains Prof. Machelska. She adds, "This led us to conclude that opioids can exert enhanced analgesia when they act directly in painful tissue -- providing that this tissue is inflamed and contain immune cells."

Exercising to avoid the flu? It’s all about the sweet spot - The Globe and Mail

a 2011 study of 1,002 adults by Dr. David Nieman at Appalachian State University found that those who exercised five or more days a week were 43 per cent less likely to develop upper respiratory tract infections during the fall and winter than those who exercised once a week or less.

Birth year dictates which flu strains make you sick

They discovered that people born before the Hong Kong flu pandemic of 1968 – in which H7N9’s ancestor, H3N2, first emerged – were largely protected from the older-type H5N1, but were vulnerable to severe illness from H7N9.
Those born after 1968 showed the opposite responses.
This explains a pattern that has puzzled scientists since 2013, when H7N9 itself was first detected: flu viruses from the H5N1 “family” disproportionately affect children and young adults, while those more closely related to H7N9 are more likely to infect older adults.

Why your muscles get less sore as you stick with your gym routine: Unexpected immune system cells may help repair muscles -- ScienceDaily

"T-cells, up until recently, were not thought to enter healthy skeletal muscle," said lead author and grad student Michael Deyhle. "We hadn't planned on measuring them because there's no evidence that T-cells play a role in infiltrating damaged muscle tissue. It's very exciting."
The presence of the T-cells suggests that muscles become more effective at recruiting immune cells following a second bout of exercise and that these cells may facilitate accelerated repair. In other words, the muscle seems to remember the damaging insult and reacts similarly to when the immune system responds to antigens--toxins, bacteria or viruses.
The group was also surprised to find inflammation actually increased after the second round of exercise. Hyldahl, his students and many physiologists have long thought inflammation goes down after the second bout of exercise, contributing to that "less sore" effect.
Instead, the slightly enhanced inflammatory response suggests inflammation itself probably does not worsen exercise-induced muscle damage.
"Many people think inflammation is a bad thing," Deyhle said. "But our data suggest when inflammation is properly regulated it is a normal and healthy process the body uses to heal itself."
Adds Hyldahl: "Some people take anti-inflammatory drugs such as Ibuprofen and Aspirin after a workout, but our study shows it may not actually be effective. The inflammation may not be directly causing the pain, since we see that muscle soreness is reduced concurrent with increases in inflammation."

"It was once believed that effector and memory cells arose as two distinct populations, with some cells initially fated to be effector type and some to be memory," McDonald said. "We've now seen that there is much more fluidity between the cell types than originally thought."
The presence of certain proteins can influence the cell's fate. Interleukin-2, for instance, is a highly inflammatory protein produced at the start of an infection.